Evidence map›Paper›PMID 27240530›Full record

ArticleMolecular psychiatry2017

Forebrain glutamatergic, but not GABAergic, neurons mediate anxiogenic effects of the glucocorticoid receptor.

J Hartmann, N Dedic, M L Pöhlmann, A Häusl, H Karst, C Engelhardt, S Westerholz, K V Wagner, C Labermaier, L Hoeijmakers and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.9field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 76 citations in OpenAlex.

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  6. SKA2 enhances stress-related glucocorticoid receptor signaling through FKBP4-FKBP5 interactions in neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  20. The glucocorticoid footprint on the memory engram.Current opinion in endocrine and metabolic research · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 3 countries.

J HartmannDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
N DedicDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
M L PöhlmannDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
A HäuslDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
H KarstDepartment of Translational Neuroscience, Brain Center Rudolf Magnus, UMC Utrecht, Utrecht, The Netherlands.
C EngelhardtDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
S WesterholzDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
K V WagnerDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
C LabermaierDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
L HoeijmakersDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
M KertokarijoDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
A ChenDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
M JoëlsDepartment of Translational Neuroscience, Brain Center Rudolf Magnus, UMC Utrecht, Utrecht, The Netherlands.
J M DeussingDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
M V SchmidtDepartment of Stress Neurobiology and Neurogenetics, Max Planck Institute of Psychiatry, Munich, Germany.
Max Planck Institute of Psychiatry · DEUniversity Medical Center Utrecht · NLHarvard University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anxiety disorders constitute a major disease and social burden worldwide; however, many questions concerning the underlying molecular mechanisms still remain open. Besides the involvement of the major excitatory (glutamate) and inhibitory (gamma aminobutyric acid (GABA)) neurotransmitter circuits in anxiety disorders, the stress system has been directly implicated in the pathophysiology of these complex mental illnesses. The glucocorticoid receptor (GR) is the major receptor for the stress hormone cortisol (corticosterone in rodents) and is widely expressed in excitatory and inhibitory neurons, as well as in glial cells. However, currently it is unknown which of these cell populations mediate GR actions that eventually regulate fear- and anxiety-related behaviors. In order to address this question, we generated mice lacking the receptor specifically in forebrain glutamatergic or GABAergic neurons by breeding GR

Indexed as

AmygdalaAnimalsAnxietyAnxiety DisordersBasolateral Nuclear ComplexCorticosteroneExcitatory Amino Acid AgentsFearGABA AgentsGABAergic Neuronsgamma-Aminobutyric AcidGlutamic AcidHypothalamo-Hypophyseal SystemMiceMice, KnockoutNeuronsCorticosteroneExcitatory Amino Acid AgentsGABA Agentsgamma-Aminobutyric AcidGlutamic AcidReceptors, GlucocorticoidReceptors, Glutamate

Identifiers

PMID27240530
OpenAlexW2410082445

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.